When dormant, perennial plants dwelling in the regions with pronounced seasonality of climate can withstand prolonged periods of harsh environmental conditions. The period of plant dormancy is commonly divided into pre-dormancy, endodormancy, and ecodormancy. During pre-dormancy, genetic, physiological, biochemical, and morphological rearrangements increasing stress resilience of the plant organism are completed. In the course of endodormancy, meristem cells cannot resume division even under favorable conditions. Environmental stimuli trigger dormancy release and the onset of ecodormancy when plant cell division and growth are restrained only by unfavorable environmental conditions. Frequent nowadays, weather fluctuations can lead to abnormal progression of dormancy. It results in the increased risk of damage to plants, especially crop plants, by adverse climatic conditions. This situation calls for the development of methods for noninvasive express monitoring of plant dormancy. Studies of the relationships between the dormancy status of plants and the functioning of their photosynthetic apparatus made possible the development of methods for monitoring of woody plant condition by recording the variable fluorescence of chlorophyll contained either in needles or in the endoderm of the shoots. This review briefly summarizes current knowledge about the mechanism of the dormancy induction and release. The functioning and regulation of the photosynthetic apparatus during winter dormancy as well as characteristic patterns of chlorophyll fluorescence induction in this period are considered. The difficulties of interpretation of chlorophyll fluorescence signals in the context of monitoring of plant dormancy are discussed together with its potential applications.

The blue-light protein sensors cryptochromes compose the widespread class of photoreceptors that regulate processes of development in plants and circadian rhythms in animals and plants. These photoreceptors can also function as magnetoreceptors. During the last decade cryptochromes have been discovered and characterized in several photosynthetic algae, where they may act not only as regulatory photoreceptors, but also as photolyases catalyzing the repair of ultraviolet-induced DNA lesions. Cryptochrome proteins bind flavin adenine dinucleotide (FAD) as a chromophore in the photolyase homology region (PHR) domain and contain the cryptochrome C-terminal extension (CCE) which is joined to PHR near the FAD-binding site. The chromophore is responsible for photosensory properties of cryptochromes and CCE is essential for their signaling activities. Photosensory processes are initiated by photochemical FAD conversions involving electron/proton transfer and the formation of redox forms. These reactions lead to changes in chromophore–protein interactions. The resulting conformational transitions in protein structure provide the molecular foundation of cryptochrome signaling activity in living systems. In plants, cryptochrome protein with photoreduced FAD undergoes conformational changes causing disengagement of the PHR domain and CCE that is accompanied by the formation of functionally active dimers/tetramers of cryptochrome molecules. Photooligomerization is considered as a key process necessary for cryptochrome signaling activity, since oligomers provide the formation their complexes with variety proteins, the components of photoreceptor signaling pathways. Interactions cryptochrome–protein in such complexes changes the protein signaling activities leading to gene expression alteration and photomorphogenesis. In this review, current knowledge on photosensory and signaling properties of cryptochromes are discussed.

A change in the diameter of small arteries and arterioles is a key mechanism for the regulation vascular bed resistance and, consequently, blood pressure and blood flow in organs and tissues. The tone of arterial smooth muscle cells (SMC) depends on the level of membrane potential (MP), which, in turn, is determined by the balance of depolarizing and hyperpolarizing ion currents. The main hyperpolarizing current of SMC is the outward potassium current. Activation and opening of potassium channels counteract depolarization, inhibit calcium entry into the cell and contraction. Thus, potassium channels play an anticontractile role in the arteries. TASK-1 channels, members of two-pore potassium channel family (K2P), have been described relatively recently in the vasculature. It is known that TASK-1 channels mediate outward potassium leakage current in arterial SMC. In addition, TASK-1 channels are regulated by a number of stimuli: their activity augments with an increase of extracellular pH, decreases at hypoxia, and can also change under the influence of inhalational/local anesthetics and vasoactive substances. TASK-1 channels play an important role in the regulation of arterial tone in pulmonary circulation, their dysfunction is one of the causes of arterial pulmonary hypertension development. In systemic arteries of adult animals, the influence of TASK-1 channels under normal pH is small or absent, but it can manifest itself under conditions of extracellular alkalosis. In addition, the anticontractile role of TASK-1 channels is more pronounced at the early period of postnatal development. This review outlines the current understanding of the functional role and regulation of TASK-1 channels in the vascular system.

Isolates of bacterial strains dominating on the surfaces of medical laboratory equipment for the selection of blood tests were obtained. Pure cultures of these bacteria are identified as Bacillus cereus HSA01, Bacillus cereus HSA12, Bacillus cereus HSA03, Bacillus subtilis HSA06, Bacillus amyloliquefaciens HSA09. The resistance of bacteria to a number β-lactam antibiotics and spectinomycin was determined. All strains are resistant to penicillin and ampicillin with a minimum inhibitory concentration (MIC) from 256 to 2048 μg/ml, as well as to cephalosporin antibiotics with a MIC value from 2 to 2048 μg/ml. Bacterial resistance to spectinomycin used in patients with allergy to penicillins and cephalosporins is in the MIC range from 16 to 256 μg/ml.
In B. cereus HSA01, resistance to ampicillin and cefuroxime is due to the operation of efflux pumps, to ceftazidime is provided by the action of metal-β-lactamases (MBL), and to penicillin is explained by the operation of both these systems. High resistance to ampicillin B. cereus HSA12 is provided by the action of MBL, to cefuroxime – by efflux activity, while resistance to ceftazidime is accompanied by the presence of MBL and the action of efflux pumps. In B. cereus HSA03, resistance to penicillin, ampicillin, cefepime, and ceftazidime is explained by efflux activity, to cefazolin and ceftazidime is provided by MBL, and to ampicillin and ceftazidime is due to the presence of both MBL and efflux. The resistance of B. subtilis HSA06 to penicillin and ampicillin is provided only by MBL activity. In B. amyloliquefaciens HSA09, resistance to ampicillin is explained by both the presence of MBL and efflux pumps, and to penicillin is provided only by the action of efflux.
Thus, in the studied group of bacilli, resistance to penicillin, ampicillin and a number of cephalosporin derivatives is provided, depending on the strain and the specific antibiotic, of metal-β-lactamase and/or efflux pumps. Pumps function due to the electrochemical potential of the cell membrane and belong to the group of secondary transporters.

One of the main reactions in the process of the light energy transformation in oxygenic organisms is the extraction of electrons from water, which are necessary for the light stage of photosynthesis. The light-dependent oxidation of water is carried out by an oxygen-evolving complex (OEC), the catalytic center of which is the cluster Mn₄CaO₅. OEC is located in photosystem II (PSII) on the lumen side of thylakoid membrane. The evolutionary origin of the PSII is unclear, as is the origin of the manganese cluster in the OEC. Recently, Johnson et al. (2013) suggested that in the primary PSII in the Archean period, the cluster Mn₄CaO₅ was absent, and PSII oxidized not water, but Mn(II) cations, i.e., manganese cations were the  source of electrons. In the presented work, we investigated the possibility of the influence of some environmental factors (citrate and hydrogen peroxide) on the oxidation rate of Mn(II) cations by a PSII that does not contain OEC. We found that citrate inhibit the oxidation of Mn(II) cations binding them but doesn’t extract Mn cations from OEC. Hydrogen peroxide, on the contrary, significantly increases the oxidation rate of manganese (from 28±2 to 145±7 μmol 2,6-dichlorophenolindophenol mg Chl^-1 h^-1 in the presence of H₂O₂). Such effects should be taken into account when investigating the oxidation of manganese cations by the photosystem as a possible source of electrons in the early stages of evolution. 

Intrauterine hypoxia is the most common prenatal risk factor providing the direct danger not only to the fetus, but also to the future postnatal life. The aim of this study is to identify the relationship between fetal hypoxia and oxidative stress, as well as to assess the significance of gestational age and gender for the development of oxidative stress. Pregnant rats were subjected to acute hypoxia on the 10th or 20th day of pregnancy, which correspond to the first and the second trimesters of human pregnancy, respectively. In newborn rats on the 2nd day of postnatal development and in mature offspring of both sexes on the 60th day of life the state of antioxidant protection was assessed by the content of non-protein thiols in blood and liver homogenate, catalase and superoxide dismutase activity in the liver homogenate, total antioxidant activity and the level of ceruloplasmin of blood plasma, as well as by the intensity of lipid peroxidation in blood plasma and liver homogenate. Regardless of the gestation period corresponding to acute hypoxia in offspring, noticeable changes of antioxidant protection system parameters were recorded in newborns, indicating the development of oxidative stress, responsible for neurological and cardiological disorders already shown for adult animals.

Neutrophils release decondensed nuclear chromatin or neutrophil extracellular traps (NET) in response to a great number of physiological and pharmacological stimuli. However, apart from the host defensive function, NETs play an essential role in the pathogenesis of various autoimmune, inflammatory, and malignant diseases. Therefore, understanding the molecular mechanisms of NET formation, usually leading to the neutrophil death (NETosis), is important to control the consequences of aberrant or excessive NET release. Protein kinase C (PKC) is a serine/threonine kinase that is involved in a variety of neutrophil functions, but its role in NETosis is not well understood. Since five PKC isoforms (α, βI, βII, δ, and ζ) have been described in human neutrophils, we studied their contribution to NETosis and oxidative burst using inhibitory analysis. Using specific PKC isoform inhibitors, we have shown that PKCβ, PKCδ, and PKCζ are involved in the oxidative burst and NETosis activated by calcium ionophore A23187, while PKCβ is involved in the oxidative burst and NETosis upon cell activation by diacylglycerol mimetic phorbol 12-myristate 13-acetate.

A technique has been developed for obtaining recombinant functionally-active peptides Ce1 and Ce4 from the venom of the scorpion Centruroides elegans in the E. coli expression system. The yields of peptides Ce1 and Ce4 were 6.5 and 12 mg per liter of culture, respectively. The properties of the obtained peptides were studied using bioengineered systems based on hybrid KV1 channels KcsA-K_v1.x (x=1, 3, 6) containing blocker binding sites of the corresponding eukaryotic potassium channels of K_v1-family. It has been shown that recombinant Ce1 and Ce4 do not exhibit affinity to the binding sites of K_v1.1 and Kv1.6 channels up to micromolar concentrations and, like natural peptides, selectively interact with the binding site of K_v1.3 channel: the apparent dissociation constants of KcsA-K_v1.3 complexes with recombinant Ce1 and Ce4 are 50±10 and 200±30 nM, respectively.

 Maternal behavior is an important factor for the offspring development in mammals. Particular traits of maternal behavior in the early ontogenesis may have a lasting effect on a number of behavioral and physiological parameters of offspring in their adulthood. In this study, we examined the maternal behavior of GC rats (GC stands for “genetic catatonics”) and control Wistar rats from the 1st to the 20th day after birth. Observations were carried out in a home cage during the day using an automated video recording system without the experimenter’s presence. GC female rats were found in the nest and nurse pups more often, as compared to the female Wistar rats. Wistar female rats “rested” outside the nest more often during the day, along with
less frequent manipulations with nest material and less frequent self-grooming. The change in the frequency of maternal behavior patterns as the offspring matures has similar dynamics in both rat strains. When comparing activity in the light and dark phases of the light/dark cycle, we found that GC females had a greater activity outside the nest at night. We assume that distinguished maternal behavior of catatonic rats may be due to greater anxiety in GC rats, as compared to control rats. 

The activity of extracellular proteinases in seven strains of different species of micromycetes of the genus Aspergillus in relation to proteins of the hemostasis system was studied. Comparison of the values of enzymatic indices during the growth of strains on agar media with casein and fibrin, followed by their submerged cultivation and analysis of amidolytic activity with chromogenic peptide substrates of proteinases of the hemostasis system, made it possible to select strains of A. candidus A4 and A. crustosus A29 as promising producers of fibrinolytic proteinases. The proteinases formed by both strains were able to cleave the chromogenic peptide substrates of thrombin, plasmin, factor X, protein C, and urokinase, exhibiting high plasmin-like and thrombin-like activity and not having an activating effect on the proenzymes of the hemostasis system.